Bottom Line:
A new study identifies an unexpected role for lysophosphatidic acid in modulating the strength of both excitatory and inhibitory synapses in the brain, but by different mechanisms.Read the accompanying Research Article.

Affiliation: Freelance Science Writer, Sherborn, Massachusetts, United States of America.

ABSTRACTA new study identifies an unexpected role for lysophosphatidic acid in modulating the strength of both excitatory and inhibitory synapses in the brain, but by different mechanisms. Read the accompanying Research Article.

pbio.1002154.g001: Membrane-derived phospholipids, such as lysophosphatidic acid (LPA), an important intermediary in lipid metabolism, are important determinants of neuron activity by regulating synaptic function.LPA induces short-term depression at both excitatory and inhibitory synapses by recruiting different signaling cascades. Because membrane-derived phospholipids, such as LPA, are intermediaries in lipids’ metabolism, these results suggest that bioactive phospholipids are potential candidates in coupling the metabolic status of the organism to brain function. Image credit: Bernardo Moreno-López.

Mentions:
Working in rodents and cultured neurons, they began by demonstrating that adding LPA at physiologic doses to excitatory neurons (those that use glutamate as a neurotransmitter) reduced the amplitude of the output current of the post-synaptic neuron, a phenomenon called short-term depression (STD). Elsewhere, LPA is known to signal through a downstream G protein, and adding an inhibitor of that protein prevented LPA’s ability to induce STD. Immunolabeling of the LPA receptor showed that it was active in the pre-synaptic neuron, where it colocalized with a marker of neurotransmitter-containing vesicles, suggesting it might exert its effect by inhibiting neurotransmitter release (Fig 1).

pbio.1002154.g001: Membrane-derived phospholipids, such as lysophosphatidic acid (LPA), an important intermediary in lipid metabolism, are important determinants of neuron activity by regulating synaptic function.LPA induces short-term depression at both excitatory and inhibitory synapses by recruiting different signaling cascades. Because membrane-derived phospholipids, such as LPA, are intermediaries in lipids’ metabolism, these results suggest that bioactive phospholipids are potential candidates in coupling the metabolic status of the organism to brain function. Image credit: Bernardo Moreno-López.

Mentions:
Working in rodents and cultured neurons, they began by demonstrating that adding LPA at physiologic doses to excitatory neurons (those that use glutamate as a neurotransmitter) reduced the amplitude of the output current of the post-synaptic neuron, a phenomenon called short-term depression (STD). Elsewhere, LPA is known to signal through a downstream G protein, and adding an inhibitor of that protein prevented LPA’s ability to induce STD. Immunolabeling of the LPA receptor showed that it was active in the pre-synaptic neuron, where it colocalized with a marker of neurotransmitter-containing vesicles, suggesting it might exert its effect by inhibiting neurotransmitter release (Fig 1).

Bottom Line:
A new study identifies an unexpected role for lysophosphatidic acid in modulating the strength of both excitatory and inhibitory synapses in the brain, but by different mechanisms.Read the accompanying Research Article.

Affiliation:
Freelance Science Writer, Sherborn, Massachusetts, United States of America.

ABSTRACTA new study identifies an unexpected role for lysophosphatidic acid in modulating the strength of both excitatory and inhibitory synapses in the brain, but by different mechanisms. Read the accompanying Research Article.